The mechanisms of poxvirus induced neoplasia and hyperplasia are not well understood. There is no evidence that integration of viral and host genome occurs, in contrast to other DNA tumor viruses. A major objective of our research is to delineate the factors responsible for induction of neoplasia by Yaba tumor virus. The factors to be examined include: (a) Examination of the role of the infected cell; that is, does the infected cell actually replicate or is cellular proliferation restricted to uninfected cells and, if the latter, how does the infected cell contribute toward induction of prolieration of uninfected cells. (b) Examination of the role of the immunologic process in possibly augmenting cellular proliferation and then ultimately controlling the same process. (c) Examination of the effects of the virion and its components (antigens) in cell physiology either as stimulating or inhibiting agents. This three-pronged approach is an outgrowth of previous studies which have provided evidence that uninfected cells are stimulated by a diffusable material released by infected cells. It is not known whether this material is a viral or cellular product and whether the host responds immunologically to it. Antigenic fractions of Yaba virus structural and associated antigens and antisera thereto are available and applicable to resolution of these problems.